Coal Workers Pneumoconioses (CWP) – Anthracosis, Silicosis and Byssinosis

Coal Workers Pneumoconioses (CWP) – Anthracosis, Silicosis and Byssinosis

Anthracosis and silicosis are major industrial problems in developing but industrialized nations since a large number of workers are engaged in mining in many states of such countries. Prolonged exposure to cola dust causes anthracosis among miners. These particles give a black color to the lesions.

Coal particles reaching the alveoli are ingested by the alveolar macrophages. The phagocytes are activated by the presence of substances like silica. Fibrosis develops at these regions. The affected lobules undergo centrilobular emphysema. On prolonged exposure, progressive enormous fibrosis (PMF) develops and this is the characteristic lesion in complicated pneumoconiosis. In radiological diagnosis, the lesions of progressive enormous fibrosis appear as sausage-shaped densities exceeding 1cm in diameter, in the upper and mid-zones of both lung fields. Further complications such as chronic bronchitis, bronchiectasis, ischemic necrosis, thrombosis of pulmonary veins, pulmonary hypertension, cor pulmonale, and lymphatic obstruction may supervene.

Clinical features

Gradual onset of dyspnea and cough with purulent expectoration mark the onset of the disease. Expectoration is more copious when bronchiectasis is also present. Dyspnea worsens when progressive enormous fibrosis supervenes. Cavitation of these lesions gives rise to expectoration of large amounts of black sputum. Large nodular lesions develop in the lungs in subjects with rheumatoid disease who develop pneumoconiosis. These lesions are 1-5cm diameter and detectable in radiological diagnosis (Caplan’s syndrome).


Prolonged exposure to dust-containing silica (silicon dioxide) gives rise to silicosis. Often this occurs in combination with anthracosis. The lesions produced by silica dust are similar to those produced by coal dust, but the lesions are larger. In addition, silicosis also gives rise to pleural thickening and adhesions. Sometimes silicosis produces acute respiratory manifestations with dyspnea and impairment of gas exchange in the alveoli.

Clinical features

In the acute form the disease manifests with dyspnea, cyanosis and constitutional disturbances. In the chronic form the noticeable manifestations are cough and hemoptysis. Physical signs may be those of bronchitis, emphysema, a pleural thickening. Silicosis predisposes the development of tuberculosis and the two diseases may coexist (silicotuberculosis). The functional impairment is a combination of restrictive and obstructive features. Immunological abnormalities such as the presence of rheumatoid factor may develop in 50% of situations.


travel military or nodular lesions are found in simple silicosis. Development of progressive enormous fibrosis leads to the presence of thick shadows in the upper zones and this is termed “complicated silicosis”. Hilar lymph nodes may show peripheral calcification.


Inhalation of asbestos dust leads to asbestosis. Asbestos is a widely used material in day-to-day life and industry. It is a complicate silicate containing silicon, oxygen, hydrogen and metals like calcium, magnesium, and iron. The raw material is obtained by mining. Different varieties of asbestos such as chrysotile, crocidolite, amosite and anthrophyllite are obtained from different regions.

Asbestos particles are needle-shaped and on account of this shape, these preferentially settle in the lower lobes. They may reach the alveoli or may be arrested at the small air passages. They give rise to alveolar epithelial hyperplasia and interstitial fibrosis. ultimately fibrosis develops around the asbestos particles and this obliterates the alveoli. Asbestos bodies are seen on histology of the lesions. These consist of asbestos fibers coated by proteinaceous material and ferritin granules derived from macrophages. Asbestos bodies may be demonstrable in the sputum. insignificant presence of asbestos bodies in sputum does not indicate that the person is experiencing from asbestosis.

Asbestosis predisposes to bronchogenic carcinoma (especially in smokers) and mesothelioma of the pleura and peritoneum. This condition also predisposes pulmonary tuberculosis. Malignancies of distant organs such as Kidneys and breasts are more shared in subjects with asbestosis.

Clinical features

The symptoms starts with increasing dyspnea on exertion, cough, malaise, and weight loss. As the condition proceeds, cyanosis and digital clubbing supervene. The functional defect is one of restriction of lung parenchyma and impairment of spread. The clinical picture differs from case to case, depending on the extent of the lesion and presence of other coexistent conditions such as emphysema, bronchiectasis, tuberculosis, malignancy or pleural disease. In Radiological examination, fine mottling and noticeable streaky fibrosis are seen in the middle and lower zones. Pleural thickening, pleural effusion, and calcification may be apparent in some situations.


Pulmonary disease caused by exposure to cotton dust, flax or hemp is termed byssinosis. In the early stages the symptoms are tightness of the chest and wheeze usually felt by the patient when he resumes work after the weekly holiday. Later on cough and dyspnea become more noticeable and persistent. Some subjects develop chronic obstructive airway disease. Persons employed in the carding section suffer more than those employed in other areas.

Cotton dust probably contains non-antigenic substances which stimulate histamine release from mast cells in the lung. Pure cotton such as surgical cotton does not provoke the symptoms. The occurrence of dyspena and cough at the beginning of the week is credited to depletion of the mast cells of their histamine. Radiological findings are nonspecific. Treatment consists of withdrawal of susceptible persons from the ecosystem and symptomatic measures. Numerous other disorders have also been recognized as resulting from occupational exposusre to different materials.


Once established, pneumoconiosis are treated symptomatically since specific therapy is lacking.


Workers who are employed in industry should be recruited only after proper medical examination. Persons with family history of allergic respiratory disorders and those who have features of obstructive airway disease are more likely to develop long-lasting ill effects. regular examination of the persons to ease early detection and removal from the unhealthy ecosystem is required by legislation. Industrial establishments where the risk of penumoconioses is present have to follow specifications intended to reduce the concentration of dust in the ecosystem and also for giving protection to the workers. Many of the penumoconioses attributable to occupational exposure are eligible for compensation from the employers.

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